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192 Chapter 5 Nephrology
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between 10 and 15% in primigravida (fi rst birth) and
5.7–7.3% in multiparas (multiple pregnancies).
Hypertension in preeclampsia is diagnosed after 20
weeks of gestation by a diastolic blood pressure >90
mmHg stable over 4 h, or one measurement of dia-
5.1
stolic blood pressure >110 mmHg. Protienuria is
defi ned as a concentration of protein of 0.1 g/L or more
in at least two random urine samples collected 4 h or
more apart; or as 0.3 g/L in a 24 h urine collection in
the absence of urinary tract infection.
Patients with preeclampsia usually present with
hypertension (hallmark of the disease), lower leg edema,
protienuria, headache, visual symptoms, and epigastric
pain. Absence of hypertension in the presence of edema
and protienuria does not exclude the diagnosis of preeclampsia. The liver is uncommonly affected by preeclampsia (10% of cases). When liver dysfunction occurs,
mild elevation of serum enzymes is common.
HELLP syndrome is a disease characterized by hemo-
lytic anemia (Hb <11 g/dL), elevated liver enzymes, low
platelets count that predispose to thrombocytopenia
(<100,000/ m L), and subcapsular liver hematoma. The
incidence of HELLP syndrome is 2–12% of preeclampsia cases. Patients often present with epigastric pain
(65%), nausea and vomiting (50%), and nonspecifi c
symptoms. Severe hypertension is not a constant or a
frequent fi nding in HELLP syndrome.
Signs on CT or MRI
In patients with HELLP syndrome, the imaging fi ndings
include subcapsular hematoma, hepatomegaly with bulging
of the left lobe, fatty liver, free abdominal ascitis, bilateral
pleural eff usions, or bilateral basal lobes atelectasis
(Fig. 5.1.13 ).
Fig. 5.1.13. Axial abdominal postcontrast CT illustration demonstrates signs of HELLP syndrome. There is hepatic subcapsular
hematoma ( solid arrowhead ), fatty liver changes ( open arrow-
head ), and ascites ( arrow )
Reversible Posterior Leucoencephalopathy
Syndrome (Hypertensive Encephalopathy)
Reversible posterior leucoencephalopathy syndrome
(RPLES) is a disease with unknown cause characterized by cerebral demyelination in the posterior white
matter areas of the brain (occipital lobes). PRLES is
thought to be caused by increased permeability of the
blood brain barrier in the posterior circulation.
PRLES is typically seen in patients with hypertension, eclampsia, and patients on immunosuppressive
and cytotoxic drugs like cephalosporine and methotrexate. PRLES is a reversible condition once the cause
is removed (e.g., control hypertension). If the cause
persists, it will lead to cerebral infarction. Patients will
present with headache, vertigo, vomiting, seizures, and
altered mental status.
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Signs on CT and MRI
On CT, there are symmetrical, noncontrast-enhancing
hypodensities located in the posterior region of the occipital
and the parietal lobes.
On MRI, symmetric low T1 signal intensity with high T2 and
FLAIR signal intensities in the region of the occipital and the
parietal lobes (Fig. 5.1.14 ).
There is cytotoxic edema and restricted water diff usion (high
DWI signal intensity) in cases of infarction.
Nephroptosis (Floating Kidney)
Nephroptosis, also known as fl oating or wandering
kidney, is a condition characterized by renal descent of
5 cm or more (or two vertebral bodies) when the patient
moves from supine to an upright position.
Nephroptosis occurs more commonly in slim
women (ten times more common than in males), and
affects the right kidney more than the left (20% of
cases). Causes of nephroptosis include multiple pregnancies, rapid loss of retroperitoneal fat, variation in
the shape of the spinal cord, shallow Gerota’s fossa,
and direct renal trauma.
Patients with nephroptosis are rarely symptomatic. Symptomatic patients typically present with history of fl ank pain in the upright position that reduces
or is relieved by lying down. The pain is attributed to
intermittent functional excretory obstruction, forceful
traction of the renal artery causing renal ischemia, or
traction of the perirenal nerves. The most severe manifestation of nephroptosis is “ Dietl’s crisis. ” Dietl’s
crisis is a condition characterized by violent paroxysmal colicky fl ank pain, tachycardia, nausea, chills,
oligouria, hypertension, and transient hematouria or
protienuria. The condition is caused by acute hydronephrosis due to kinking or vascular obstruction of the
ureters.
On physical examination, the lower pole of the kidney can be palpated on deep inspiration. The examiner’s fi nger should reach over the upper pole of the
kidney and push it down to the navel. On Dietl’s crisis,
the kidney is tender on palpation and may be enlarged.
Historically, nephroptosis is used to be corrected by
nephropexy , a surgical procedure characterized by
suturing part of the renal capsule to the surrounding
abdominal wall and vertebral column.
Signs on IVU
IVU is the classical diagnostic investigation for nephroptosis.
The patient is injected with the contrast intravenously, and
the kidney is imaged after opacifi cation of the renal
parenchyma and ureters while the patient is supine. The
patient is then imaged while he is on erect position. The
kidney is clearly seen descending caudally from its normal
position between the two fi lms (e.g., from the level of L2 to
the level of L5). The normal kidney is located between the
lumbar vertebral levels L1 to L4.
Fig. 5.1.14. Axial T1W ( a )
and T2W ( b ) MR-illustrations
demonstrate bilateral almost
symmetrical low T1 and high
T2 signal intensity lesions
located in the posterior lobes.
This sign with a history of
hypertension is diagnostic of
RPLES
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Signs on Doppler Sonography
In suspected cases of nephroptosis, the resistive indexes (RIs)
of the interlobar parenchyma renal arteries should be
5.1
measured on both supine and erect positions. Both kidneys
should be imaged for comparison. In the ptotic kidney, there
is a change in the RI values >0.1 between the erect and
supine examinations (e.g., on supine it is 0.5, and on erect it
is 0.6). The other normal kidney shows no change in the RI
values on both supine and erect examinations. These fi ndings
are explained by the renal artery tension occurring due to
downward movement of the kidney.
Riley-Day Syndrome
(Familial Dysautonomia)
Riley-Day syndrome (RDS) is a rare inherited disorder
characterized by infantile hypertension, postural
hypotension, and recurrent attacks of unexplained
fever due to autonomic nervous system dysfunction.
As a rule, RDS manifests in infancy, which is
important to assume the diagnosis. The major features
are often seen in an infant or a child with recurrent
attacks of unexplained fever, hypertension, and vomiting. Infants commonly have excessive drooling with
swallowing diffi culties, making them prone to recurrent aspiration pneumonia. Aspiration pneumonia is
the main cause of death in patients with RDS.
Hypertension of RDS is characteristically associated with excitement. Intermittent attacks of hypertension with vomiting may cause RDS to be confused
with infantile pheochromocytoma. Postural hypotension can be demonstrated in most patients beyond 2
years of age, and it can be so marked as to give raise to
“blackout spells” when the patient stands.
Stafne’s Bone Defect of the Mandible
Stafne’s bone defect of the mandible is a rare cyst-like
bony defect with cortical bone thickening with continuity from the base of the mandible around the gonial
angle of the mandible, under the mandibular canal on
panoramic radiography or cone-beam CT. Most cases
are seen in hypertensive patients from 40 to 60 years
old. The bony defect is symptomless.
Fig. 5.1.15. Axial CT illustration of the mandible demo
nstrates Stafne’s bone defect of the mandible on the right side
( arrowhead )
Stafne’s mandibular bony defect is considered as a
complication of long-standing hypertension, and
thought to be caused by high pressure exertion by the
facial artery over the mandible (Fig. 5.1.15 ).
Hypertensive Heart Disease
Patients with long-standing hypertension develop left
ventricle hypertrophy due to raised left ventricular
wall tension, which may lead to coronary microangiopathy of the mid-wall portion of the left ventricle
wall. Hypertensive heart disease is a term used to
describe a hypertensive patient with cardiac failure due
to diastolic heart dysfunction with normal systolic
heart function (normal ejection fraction).
Left ventricular hypertrophy can be generalized
reducing the internal cavity (concentric hypertrophy),
or localized to the interventricular septum (eccentric
hypertrophy). Left ventricular hypertrophy in hypertensive patients is usually concentric, and typically found
in moderate to severe hypertension in middle-aged and
elderly patients. Left ventricular hypertrophy can cause
atrial fi brillation and arrhythmias. Also, left ventricular
hypertrophy in hypertensive patients is associated with
three- to fourfold increase in the risk of stroke, a two- to
threefold increase in coronary heart disease, and a threefold increase in peripheral arterial disease.
5.1 Hypertension 195
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Signs on Cardiac MRI
Patients with left ventricular hypertrophy due to hypertensive
heart disease can show intra-mural, mid-wall, or subendocardial
delayed contrast enhancement (e.g., >15 min), mostly due to
myocardial ischemia, necrosis, or fi brosis (Fig. 5.1.16 ). Patients
with delayed contrast enhancement on cardiac MRI may show
ST-segment depression or T-wave inversion on electrocardiogram.
Fig. 5.1.16. Short-axis dark-blood postcontrast cardiac
MR-illustration demonstrates left ventricular concentric hypertrophy with intramural enhancement representing MR fi ndings
in hypertensive heart disease
For Further Reading
1 . Hartman RP et al Evaluation of renal causes of hyperten-
sion. Radiol Clin N Am. 2003;41:909–29
2 . Chen Pet al Color and power Doppler imaging of the kid-
neys. World J Urol. 1998;16:41–5
3 . Soulez G et al Imaging of renovascular hypertension:
Respective values of renal Doppler US, and MR angiography. RadioGraphics. 2000;20:1355–68
4 . Olivier H et al Renovascular disease: Doppler ultrasound.
Semin Ultrasound CT MRI. 1997;18(2):136–46
5 . Ha HK et al Radiologic features of vasculitis involving the
gastrointestinal tract. RadioGraphics. 2000;20:779–94
6 . Rooholamini SA et al Imaging of pregnancy-related com-
plications. RadioGraphics. 1993;13:753–70
7 . Dineen R et al Imaging of acute neurological conditions in
pregnancy and the puerperium. Clin Radiol. 2005;60:
1156–70
8 . Ferrazzani S. Hypertension in pregnancy. Saudi J Kidney
Dis Transplant. 1999;10(3):298–312
9 . Strohmeyer DM et al Changes of renal blood fl ow in neph-
roptosis: assessment by color Doppler imaging, isotope
renography and correlation with clinical outcome after
laparoscopic nephropexy. Eur Urol. 2004;45:790–93
10 . Hoenig DM et al Nephroptosis: a “disparaged” condition
revisited. Urology. 1999;54:590–96
11 . Moss SW. Floating kidneys: a century of nephroptosis and
nephropexy. J Urol. 1997;158:699–702
12 . Barber NJ et al Nephroptosis and mephropexy - hang up on
the past? Eur Urol. 2004;46:428–33
13 . Taneja K et al Pseudocoarctation of the aorta: complemen-
tary fi ndings on plain fi lm radiography, CT, DSA, and MRA.
Cardiovasc Intervent Radiol. 1998;21:439–41
14 . Son JS et al Pseudocoarctation of the aorta associated with
the anomalous origin of the left vertebral artery: a case
report. Korean J Radiol. 2008;9:283–85
15 . Applegate KE et al Spontaneous colonic ischemia in a
patient with Riley-Day syndrome. Pediatr Radiol. 1995;25:
312–13
16 . Akpunonu BE et al Secondary hypertension: evaluation and
treatment. Dis Mon. 1996;42(10):609
17 . Lewis VD III et al The midaortic syndrome: diagnosis and
treatment. Radiology. 1988;167:111–13
18 . Das BB et al Midaortic syndrome presenting as neonatal
hypertension. Pediatr Cardiol. 2008;29:1000–1
19 . Stadlmaier E et al Midaortic syndrome and celiac disease: a
case of local vasculitis. Clin Rheumatol. 2005;24:301–4
20 . Fujita T et al Takayasu arteritis evaluated by multi-slice
computed tomography in old man. Int J Cardiol. 2008;125:
286–87
21 . Canyigit M et al Imaging characteristics of Takayasu arteri-
tis. Cardiovasc Intervent Radiol. 2007;30:711–18
22 . Ando H et al Abnormal collateral arterial system in
Takayasu’s arteritis and Lariche’s syndrome evaluated by
whole body acquisition using multislice computed tomography. Int J Cardiol. 2007;121:306–8
23 . Bulum J et al Takayasu’s arteritis and chronic autoimmune
thyroiditis in a patient with type 1 diabetes mellitus. Clin
Rheumatol. 2005;24:169–71
24 . Dyer RB et al Classic signs in uroradiology. RadioGraphics.
2004;24:S247–80
25 . Shimizu M et al CT analysis of the Stafne’s bone defects of
the mandible. Dentomaxillofacial Radiol. 2006;35:95–102
26 . Van Hoe L et al Liver involvement in HELLP syndrome: CT
and MRI fi ndings in two patients. Eur Radiol. 1995;5:331–34
27 . Andersen K et al Myocardial delayed contrast enhancement
in patients with arterial hypertension: initial results of cardiac MRI. Eur J Radiol. 2009;71:75–81
28 . Lip GYH et al Hypertensive heart disease. A complex syn-
drome or a hypertensive ‘cardiomyopathy’? Eur Heart
J. 2000;21:1653–65
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5.2
5.2
Polycystic Kidney Disease
Polycystic kidney disease (PKD) is a disease characterized by development of multiple cysts within the
kidneys in bilateral fashion. A cyst is defi ned as a fl uidfi lled sac lined with a single layer of tubular epithelium. A cystic kidney is defi ned as a kidney that
contains three or more cysts.
Simple renal cyst is the most common renal anomaly. Up to 22% of symptomless patients over 70 years
old or older have at least one renal cyst. There are three
types of PKD: autosomal dominant (adult) PKD, autosomal recessive (infantile) PKD, and acquired PKD.
Autosomal Dominant Polycystic
Kidney Disease
Autosomal dominant polycystic kidney disease
(ADPKD) is the fourth cause of chronic renal failure
through the world. The disease has an autosomal dominant mode of inheritance as its name states, with a
positive family history of ADPKD elicited in 60% of
patients.
ADPKD is typically seen in adults, with both kidneys affected in a bilateral, almost symmetrical, fashion. The kidneys are enlarged in size as the disease
progresses. In a patient <30 years old with a positive
family history of ADPKD, the presence of two cysts,
either unilateral or bilateral, is suffi cient to make the
diagnosis. In patients >30 years old with a positive
family history of ADPKD, at least two cysts in each
kidney are suffi cient to make the diagnosis.
Patients with ADPKD present with bilateral renal
cysts with enlarged kidneys (100%), renal pain
(60%), hematuria (42%), hypertension (75%), colonic
diverticuli (80%), and hepatic cysts (57%). Potential
causes of hematuria in ADPKD include renal stones
formation (20%), and golmerulonephritis.
Hypertension arises in 75% of ADPKD with normal renal functions. Cyst expansion is believed to alter
blood fl ow by glomerular compression, which results
in the release of rennin, leading to the formation of
angiotensin II.
Hepatic cysts occur in 57% of patients with ADPKD,
and they are rare before puberty. Hepatic cysts are
believed to originate from cystic dilatation of the bile
ducts. Patients may present with right upper quadrant
pain due to liver capsule stretching and hepatomegaly.
Colonic diverticuli are seen in up to 80% of patients
with ADPKD, usually with end-stage renal disease.
Patients with ADPKD are at risk of cerebral aneurysm
rupture, which has a prevalence of <5%. ADPKD
patients with positive family history of cerebral arteries aneurysm have an increased incidence of developing cerebral aneurysm (22%) than ADPKD patients
with no family history of cerebral aneurysm (5%).
ADPKD patients with aneurismal rupture present with
signs of intracranial bleeding or subarachnoid hemorrhage such as severe headache, neck stiffness, altered
consciousness, with nausea and vomiting.
Rare manifestations of ADPKD include coronary
arteries or abdominal aorta aneurysm, mitral valve
prolapse, aortic regurgitation, pancreatic cysts (10%),
splenic cysts (5%), and inguinal hernias. Patients with
ADPKD may develop seminal vesicle cysts, which
present clinically as painful ejaculation, prostatitis,
urinary tract obstruction, or epididymitis.
Signs on US
The kidneys show multiple echo-free parenchymal cysts with
typical posterior shadowing.
Liver, pancreatic, or splenic cysts may be seen (Fig. 5.2.1 ).
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Fig. 5.2.1. Axial CT postcontrast ( a ) with liver ultrasound ( b ) images show multiple liver cysts in a patient with ADPKD
Signs on CT
Typically, both kidneys are enlarged with multiple cysts of
variable sizes (Fig. 5.2.2 ).
Hyperdense calculi may be seen within the renal pelvis or the
ureters.
Hepatic, pancreatic, or splenic cysts may be seen (Fig. 5.2.1 ).
Intrahepatic cystic bile duct dilatation (Caroli’s disease) can be
associated with PKD in up to 70% of cases.
Fig. 5.2.2. Axial CT urography image in a patient with ADPKD
shows bilateral mildly enlarged kidneys with multiple cysts
Signs on MRI
Cerebral MR-angiography should be performed for ADPKD
patients with positive family history of cerebral aneurysms as
a screening examination. These aneurysms are classically
saccular aneurysms that occur at the bifurcation of cerebral
vessels, and resemble a berry in size and shape ( berry
aneurysm ). Up to 80% of berry aneurysms arise from the circle
of Willis, and 20% arise from the posterior fossa.
Seminal vesicle cyst is detected as unilocular cyst with
fl uid-signal located at the posterolateral aspect of the urinary
bladder. The cyst may be associated with ipsilateral
ejaculatory duct dilatation that may protrude into the urinary
bladder mimicking ectopic uretrocele.
Autosomal Recessive Polycystic
Kidney Disease
Autosomal recessive polycystic kidney disease
(ARPKD) is a rare genetic disease with prevalence of
1:20,000 live births. ARPKD typically starts in neonates and infants as early renal failure. Infant’s death
usually occurs within the fi rst year of life, unless renal
transplantation is considered.
The kidneys are massively enlarged with numerous
cysts. Hepatic fi brosis is very common in ARPKD
(60%). Hypertension occurs in almost all cases.
Pregnant women with an infant with ARPKD typically
display oligohydramnios.
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5.2
Signs on CT
Both kidneys are massively enlarged while maintaining a
reniform shape (Fig. 5.2.3 ).
Acquired Polycystic Kidney Disease
Acquired polycystic kidney disease (APKD) is typically seen in chronic renal failure and dialysis. Chronic
potassium depletion in humans has been associated
with the development of renal cysts (e.g., primary
Hyperaldosteronism). Some investigators use the term
“multiple cystic kidney disease” for this condition to
differentiate it from the true congenital polycystic kidney disease.
In contrast to ADPKD and ARPKD, the kidney size
is usually normal or smaller than normal. Also, the
acquired polycystic kidney has a tendency for malignant transformation.
Signs on CT
Bilateral normal size or shrunken kidneys with multiple cysts
(Fig. 5.2.4 ).
Signs of other complication of end-stage disease, or adrenal
hyperplasia (hyperaldosteronism) may be seen.
Fig. 5.2.3. Axial ( a ) and coronal ( b ) CT urography images in a
child with ARPKD show massively enlarged kidneys with
numerous small cysts bilaterally
Fig. 5.2.4. Axial CT urography in a patient with acquired polycystic kidney disease shows bilateral normal-sized kidneys with
small cysts
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D i ff erential Diagnoses and Related Diseases
Nephronophthisis is an uncommon autosomal dominant
disorder characterized by a triad of anemia, salt-wasting, and abnormal levels of nitrogen-containing compounds like urea and creatinine (azotemia) due to
tubulo-interstitial nephritis. Patients are usually young
adults or children presenting with end-stage renal failure. Due to its nonspecifi c symptoms, defi nite diagnosis
is usually established by kidney biopsy, which classically shows tubular basement membrane disintegration,
tubular cyst formation, and tubulo-interstitial fi brosis.
The disease has three forms: infantile, juvenile, and
adolescent. Nephronophthiasis can be associated with
retinitis pigmentosa (Senior-Løken syndrome), cerebellar ataxia and cerebellar vermis hypoplasia (Joubert’s
syndrome), oculomotor apraxia (Cogan’s syndrome),
hepatic fi brosis and biliary duct proliferation (Boichis
syndrome), phalangeal cone-shaped epiphysis (SaldinoMainzer disease/conorenal syndrome), hypopituitarism
(RHYNS syndrome), ectodermal dysplasia (Sensenbrenner syndrome), and leber amaurosis (ArimaDekaban syndrome). Brain MRI shows the characteristic
“molar tooth sign” due to superior cerebellar vermis
hypoplasia of Joubert’s syndrome. On ultrasound,
kidneys show multiple cysts up to 2 cm in size,
characteristically located at the renal medulla, with
hyperechoic cortex and loss of the cortico-medullary
differentiation. Many researches consider the clinical
presentation of nephronophthisis with ultrasound picture of medullary renal cysts as being characteristic and
suffi cient to establish the diagnosis without the need for
renal biopsy. However, renal medullary cysts may be
absent in 30% of cases, so the absence of medullary
renal cysts does not rule out the diagnosis.
For Further Reading
1 . Martinez JR et al Polycystic kidney disease: etiology, patho-
genesis and treatment. Dis Mon. 1995;41(11):693–765
2 . Capisonda R et al Autosomal recessive polycystic kidney
disease: outcomes from a single-center experience. Pediatr
Nephrol. 2003;18:119–26
3 . Vauthey J-N et al Adult polycystic disease of the liver. Br
J Surg. 1991;78:542–527
4 . Roche CJ et al Selections from the buffet of food signs in
radiology. RadioGraphics. 2002;22:1369–84
5 . Salomon R et al Nephronophthisis. Pediatr Nephrol.
(2009);24:2333–2344
6 . Blowey DL et al Ultrasound fi ndings in juvenile nephro-
nophthisis. Pediatr Nephrol. 1996;10:22–4
7 . Grossman H et al Sonographic diagnosis of renal cystic
diseases. AJR. 1963;140:81–5
Chapter 6
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Endocrinology and Metabolism
CONTENTS
6.1 Grave’s Disease (Hyperthyroidism) 202
6.2 Hyperparathyroidism 204
6.3 Growth Hormone Diseases 210
6.4 Osteoporosis 217
6.5 Rickets and Osteomalacia 222
6.6 Scurvy 225
6.7 Fluorosis 227
6.8 Lead Poisoning (Plumbism) 230
6.9 Adrenal Glands Abnormalities 231
6.10 Sex Hormones Abnormalities 238
6.11 Sheehan Syndrome (Postpartum Hypopituitarism) 247
J. A. Al-Tubaikh: Internal Medicine – An Illustrated Radiological Guide
DOI: 10.1007/978-3-642-03709-2_6 © Springer-Verlag Berlin Heidelberg 2010
201
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6.1
6.1
Grave’s Disease (Hyperthyroidism)
Graves’s disease (GD) is an autoimmune disorder characterized by hyperthyroidism, thyroid goiter, and ophthalmopathy. The disease arises due to the production of
autoantibodies that auto-stimulates the thyrotropin receptors in the thyroid gland to secrete thyroid hormones.
GD clinical manifestations are mainly due to hyperthyroidism (thyrotoxicosis). Patients are commonly
females between the third and fi fth decades presenting
with thyroid goiter. The thyroid is hypervascular, with
venous humming that can be heard by stethoscope in
some cases.
Systemic manifestations of hyperthyroidism include
rapid weight loss (>10% of body weight in less than 6
months), profuse sweating and heat intolerance,
increased appetite (85%), anorexia (15%), increased
bowel motion and diarrhea, oligomenorrhea in females,
gynecomastia in males due to increased sex-hormone
binding proteins, and proximal muscle weakness and
muscle wasting due to increased basal metabolic rate.
Skin manifestations include skin moisture due to
sweating, vitiligo, and pretibial skin thickening due to
mucin deposition in the dermis (myxoedema).
Graves’ ophthalmopathy is the most characteristic
sign of this disease. GD is the most common cause of
exophthalmos (abnormal prominent eye) and proptosis
(protrusion) of globe in adults. It occurs in 35% of
cases. The proptosis can precede the actual thyroid
abnormalities or occur after the disease has been brought
under control. Proptoses are commonly bilateral and
symmetrical; unilateral proptosis is uncommon.
Proptosis in GD can be explained by:
Clinical signs of Graves’ ophthalmopathy include
widened palpebral fi ssure ( Dalrymple’s sign ), staring
expression with infrequent blinking ( Stellwag’s sign ),
lid lag on downward gaze ( von Graefe’s sign ), and
poor convergence ( Möbius’s sign) . Up to 5% of patients
with Graves’ ophthalmopathy develop optic neuropathy due to compression of the nerve in its canal because
of backward herniation of the retro-orbital fat through
the optic canal, or from hypertrophied ocular muscle
belly at the orbital apex.
Signs on US and Doppler Sonography
The gland is diff usely hypoechoic and enlarged in size.
On color Doppler scan, the gland shows bilateral diff use increase
duplex signal due to hypervascularity. This sign is characteristic for GD and is called “thyroid inferno” sign (Fig. 6.1.1 ).
Signs of Graves’s Ophthalmopathy on CT
and MRI
Bilateral, symmetrical increase in orbital muscles bellies width
with spares tendons causing the orbital muscles to have
fusiform appearance. The inferior rectus and the medial rectus
muscles are characteristically aff ected (Figs. 6.1.2 and 6.1.3 ).
Increases in the retrobulbar fat size.
CT evidence of proptosis is defi ned as globe protrusion
exceeding the interzygomatic line by 21 mm or more on axial
images at the level of the lens (Fig. 6.1.4 ).
I n fi ltration and deposition of mucopolysaccharido-
sis (hyaluronic acid) into orbital muscles. The muscles’ bellies are characteristically increased in size
while their tendons are spared (fusiform enlargement). The inferior rectus and the medial rectus
muscles are the most commonly involved. The lateral rectus is the last muscle to be involved.
Hypertrophy of the lateral rectus only can be seen in
orbital pseudotumor, and hypertrophy of the superior rectus only can be seen in orbital lymphoma.
Increased volume of the retrobulbar fat which will
push the globe anteriorly.
Fig. 6.1.1. Color Doppler (Duplex) scan of the thyroid in a
patient with Grave’s disease shows marked vascular signal due
to bruit (thyroid inferno sign)
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